News
Scientists urge action on plastic additives linked to sperm decline
Scientists have warned that chemicals in plastics are driving falling sperm counts, after talks on a global pollution treaty collapsed over disputes about chemical regulation.
Last week, after nearly two weeks of negotiations, delegates left Geneva on Friday without agreement, after oil- and gas-producing nations objected to production limits and chemical curbs.
Almost 100 nations signed a declaration calling for a “legally binding obligation to phase out those most harmful plastic products and chemicals of concern”.
But both texts drafted by Luis Vayas Valdivieso, chair of the negotiating committee, omitted any reference to chemical controls.
Global sperm counts have dropped by about one per cent each year for 50 years, with fertility declining at similar rates, studies show.
Obesity, sedentary lifestyles and ageing populations have been cited as possible causes, but reproductive health experts say environmental factors are most significant.
Dr Shanna Swan, professor of environmental medicine and public health at the Icahn School of Medicine at Mount Sinai in New York City, said the decline was “largely, but not entirely due to toxins in the environment that have the ability to interfere with steroid hormones”.
In 2017, Swan and colleagues published a meta-analysis showing sperm counts had fallen by nearly 60 per cent among men in North America, Europe and Australia between 1973 and 2011.
When they repeated the research in 2023, extending the period to 2018 and adding data from Africa, Asia and South America, the findings were even more shocking.
Swan said: “We separated the countries into western and non-western for analytic purposes, and in both we found a significant decline.
“And the other thing that we found, which was at least as alarming, was that if you looked at all of the studies going back to 1973 you see a one per cent per year decline.
“But if you look at studies published after 2000, you see an over two per cent decline.
“So the rate of decline had increased, and had increased significantly in recent years.”
The warning comes after a report published two weeks ago by Deep Science Ventures, reviewed by Swan, described chemical pollution as “a threat of a similar order as climate change”, though it receives far less attention.
Falling sperm rates since around 1950 correlate with rising plastics use. Swan highlighted strong evidence linking common plastic additives to reduced sperm counts.
Swan explained: “Phthalates are chemicals that are put into plastic to give it flexibility and make it soft and flexible.
“So any time you pick up a soft water bottle or tubing, like medical tubing, or a food container that’s soft, you’re going to be touching phthalates.
“Then, on the other side, the evil twin of phthalates are the bisphenols.
“While phthalates make plastic soft and flexible, bisphenols make it hard and inflexible. And phthalates lower testosterone and the bisphenols increase oestrogen.”
These endocrine-disrupting chemicals – substances that disturb hormone systems – particularly affect foetuses and embryos developing in the womb.
Swan had previously studied the effects of phthalates on unborn male babies, finding that exposure at critical points in pregnancy could cause subtle deformities in sexual development.
The adverse effects, known as “phthalate syndrome”, included smaller penises, a shorter distance between the genitals and anus, and, later in life, lower sperm counts at sexual maturity.
“We showed the link between the exposure and fertility,” Swan said.
“And when you see that total sperm count going down worldwide, what I believe is you’re seeing an important effect of early exposure to these chemicals.”
Swan would not be drawn into commenting on the treaty talks under way in Geneva, but said urgent action was needed on plastic additives and safer replacements.
She said: “In the meantime, yes people can be careful,.
“They can reuse materials. They should try to look at what they use in their takeout containers and carry little glass bottles around to get their drinks.
“It’s very important. But it’s not solving a bigger problem, which is how do we make these things that we have become dependent on in a safer way?”
Diagnosis
Lung cancer drug shows breast cancer potential
Ovarian cancer cells quickly activate survival responses after PARP inhibitor treatment, and a lung cancer drug could help block this, research suggests.
PARP inhibitors are a common treatment for ovarian cancer, particularly in tumours with faulty DNA repair. They stop cancer cells fixing DNA damage, which leads to cell death, but many tumours later stop responding.
Researchers identified a way cancer cells may survive PARP inhibitor treatment from the outset, pointing to a potential way to block that response. A Mayo Clinic team found ovarian cancer cells rapidly switch on a pro-survival programme after exposure to PARP inhibitors. A key driver is FRA1, a transcription factor (a protein that turns genes on and off) that helps cancer cells adapt and avoid death.
The team then tested whether brigatinib, a drug approved for certain lung cancers, could block this response and boost the effect of PARP inhibitors. Brigatinib was chosen because it inhibits multiple signalling pathways involved in cancer cell survival.
In laboratory studies, combining brigatinib with a PARP inhibitor was more effective than either treatment alone. Notably, the effect was seen in cancer cells but not normal cells, suggesting a more targeted approach.
Brigatinib also appeared to act in an unexpected way. Rather than working through the usual DNA repair routes, it shut down two signalling molecules, FAK and EPHA2, that aggressive ovarian cancer cells rely on. FAK and EPHA2 are proteins that relay survival signals inside cells. Blocking both at once weakened the cells’ ability to adapt and resist treatment, making them more vulnerable to PARP inhibitors.
Tumours with higher levels of FAK and EPHA2 responded better to the drug combination. Other data link high levels of these molecules to more aggressive disease, pointing to potential benefit in harder-to-treat cases.
Arun Kanakkanthara, an oncology investigator at Mayo Clinic and a senior author of the study, said: “This work shows that drug resistance does not always emerge slowly over time; cancer cells can activate survival programmes very early after treatment begins.”
John Weroha, a medical oncologist at Mayo Clinic and a senior author of the study, said: “From a clinical perspective, resistance remains one of the biggest challenges in treating ovarian cancer. By combining mechanistic insights from Dr Kanakkanthara’s laboratory with my clinical experience, this preclinical work supports the strategy of targeting resistance early, before it has a chance to take hold. This strategy could improve patient outcomes.”
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